Physicians Office Resource Volume 8 Issue 08 | Page 25

PHYSICIANS OFFICE NEWS BRIEFS
combination of congenic mapping, in silico
haplotype analyses, and comparative genomics.
Among different mouse strains, sequence
variants of Inpp4b were identified, and these
correlated with differences in individual cortical
MEP latency. Transgenic mice carrying the longerlatency allele (Inpp4b474R/548P) in the C57BL/6J
background exhibited significantly longer
cortical MEP latencies. In German and Spanish
multiple sclerosis cohorts, an association of an
INPP4B polymorphism (rs13102150) was
observed with multiple sclerosis.
"This study reports an interesting
observation, but the neurobiological
mechanisms, which provide a clear picture of
why INPP4B impairs conduction velocity
remain unclear," writes Hans Lassmann, M.D.,
from the Medical University of Vienna, in an
accompanying editorial.

the types of organizational structures -- such as
independent practice associations -- that may
make it possible for small practices to share
resources that are useful for improving the quality
of care," Casalino and colleagues conclude.

G

ene ID'd Which Regulates
Nerve Conduction Velocity
A novel gene has been identified
as having a regulatory role in
nerve conduction velocity,
according to an experimental study published
online Aug. 12 in The Journal of Pathology.
Using a classical genetic approach,
Susanne Lemcke, Ph.D., from the University of
Lübeck in Germany, and colleagues examined
novel genes controlling nerve conduction.
The researchers identified EAE31, a locus
controlling latency of motor evoked potentials
(MEPs) and clinical onset of experimental
autoimmune encephalomyelitis, using
quantitative trait mapping in F2 progeny of B10/
SJL mice. The quantitative trait gene for EAE31
was identified as inositol polyphosphate-4phosphatase type II (Inpp4b), using a

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